Spasticity is a common complication of hemispheric stroke, impacting 40% or more of stroke survivors. Its most visible clinical feature is muscular hypertonia, or increased resistance of a limb to externally imposed motion. If left untreated, this increase in tone can impede joint motion, limiting recovery of voluntary movement. In addition, spasticity may lead to persistent muscle shortening, giving rise to joint deformity, and to muscle contracture. The pathophysiology appears to depend on an enhancement of the stretch reflex response, but we do not know where this enhancement originates. Accordingly, this proposal seeks to explore the physiological origins of spastic hypertonia by examining several alternative hypotheses about the basic underlying mechanisms. First, there could be greater excitatory synaptic drive to the spinal motoneuron pool, arising from key descending spinal pathways such as the vestibulospinal and/or reticulospinal tracts. Second, there could be larger, and/or longer-duration Ia excitatory synaptic potentials (EPSP'S) in spinal motoneurons elicited by the muscle stretch. Third, there could be changes in the intrinsic membrane properties of motoneurons such as in voltage-gated conductances of motoneurons, giving rise to persistent inward currents, or PIC's. We plan to explore these mechanisms in hemispheric stroke survivors, using advanced EMG recording technologies, coupled with the use of a novel tendon probe (the Linmot), which imposes controlled muscle length changes on the muscle (the biceps muscle) and records biceps muscle force. These approaches, when combined, should allow us to separate the relative contributions of the proposed mechanisms, and should help us to develop greater diagnostic precision about the physiological characteristics of spasticity, as well as to design novel therapeutic approaches.